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X Pediatrics 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Endocrine portion of pancreas

A

Islet of Langerhans (mostly full of B cells that secrete insulin)

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2
Q

Normal physiology of glucose

A

High glucose stimulate insulin release from B cells

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3
Q

Pathophysiology of DM1

A

Destruction of pancreatic B cells (mostly autoimmune and rest are idiopathic) leads to decreased insulin secretion and hyperglycemia

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4
Q

2 peaks of type 1 DM

A

Mid childhood (age 4-6) and early puberty (10-14)

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5
Q

Incidence of DM in the world

A

Colder population and further from the equator has an increased incidence

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6
Q

Non-modifiable risk factors of type 1 DM

A

White population is highest

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7
Q

Possible environmental risk factors of type 1 DM

A

Viral infections (EBV, Coxsackier, CMV)
Diet
Higher socioeconomic status
Obesity

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8
Q

Diet risk factors for type 1 DM

A

Increased risk with exposure to cows milk and early cereal introduction
Decreased risk with breastfeeding and solid food at later ages

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9
Q

3 presentations of type 1 DM

A

Classic (3 Ps and weight loss/fatigue)
DKA (fruit smelling, drowsy)-hospitalize, hydrate, insulin
Silent (incidental) discovery

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10
Q

Diagnostic criteria of type 1 DM

A

Fasting plasma glucose >126
Random plasma glucose >200 mg/dL
(Plasma glucose >200 2 hrs after oral glucose tolerance test
HbA1C >6.5)

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11
Q

What to do when kid presents with type 1 for first time or DKA?

A

Hospitalize

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12
Q

Common sxs of hypoglycemia

A

Irritability, shaking, dizziness, sweating, nausea

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13
Q

Goals of type 1 tx

A

Achieve glucose control without hypoglycemia (higher risk when 4,5 and 6)–decreased risk when get older
Set goals

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14
Q

Target for ideal fasting blood glucose and HbA1C based on age

A

<5: 80-200 and 7.5-8.5%
6-11: 70-180 and <8%
12-19: 70-150 and <7.5%

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15
Q

Types of insulin

A 
Rapid acting (lispro, aspart)
Short acting (regular insulin)- pre meal bolus 5-30 min before meal
Intermediate acting (NPH insulin)-combo with long
Long-acting (glargine, detemir) administer 1-2x/day
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16
Q

Which insulins are used to combat a significant increase in blood glucose?

A

Rapid and short acting

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17
Q

Physiologic regimen for insulin dosing

A

Basal: intermediate or long acting to suppress hepatic glucose production
Bolus: rapid or short acting to cover carb intake at meals
1 unit per kilo over 24 hrs (half and half)

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18
Q

Definition of obesity

A

Normal is 5th-85th percentile
Overweight is 85-95th percentile
Obese is >95th percentile
Severe obesity is >120th

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19
Q

When is obesity more common ethnically?

A

American Indian, black and Mexican Americans

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20
Q

What is a strong predictor of adult obesity?

A

Childhood obesity

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21
Q

General nutrition recommendations

A 
Stabilize weight or small weight loss is obese
Portion control
Avoid sugary drinks
Limit milk intake (after 1)
900-1200 kcal/day when 6-12
Eat at home
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22
Q

Exercise recommendations

A

30-60 min of activity per day

Non-academic screen time to 2 hrs per day

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23
Q

Risk factors of type 2 DM

A

Obesity
Family hx
Native American, African American, Latino, Asian American or Pacific Islander
Conditions associated with insulin resistance

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24
Q

Sxs of type 2

A 
Polydipsia and polyuria
Visual disturbances
Infections
Most are asymptomatic
Fatigue, irritable, can't concentrate
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25
Q

Acanthosis nigricans

A

Risk factor for type 2 (excess keratin makes skin thicker due to receptors for insulin)

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26
Q

When do you screen for type 2 DM in kids?

A

Screen kids >10 YO if overweight/obese AND have 2 or more of following:
type 2 DM in first or second degree
high risk ethnic group
signs of insulin resistance
maternal hx of DM or gestational diabetes when kid in utero
*every 3 yrs

27
Q

Tx for type 2 overview

A 
Lifestyle
Treat psychosocial aspects
Metformin and insulin
Prevent macro and microvascular complications
Comorbidities
28
Q

First line tx type 2

A

Metformin

29
Q

When is insulin recommended along with metformin and lifestyle changes?

A

Random plasma glucose >250 or HbA1C>9%

30
Q

Monitoring for type 2

A

Review weight, DMI, diet and activity
Blood glucose monitoring 3/day on insulin
Monitor A1c every 3 mos
Lab tests for HTN and hyperlipidemia

31
Q

First line tx for HTN with type 2 DM

A

ACE-i or ARBs

second is thiazides, CCBs or BBs

32
Q

Why do we not like BB for DM?

A

Masks sxs of hypoglycemia

33
Q

Stages of HTN

A

Stage 1 is 130/80-139/89

Stage 2 is >140/90

34
Q

Goals for lipid levels in adolescents in DM

A

LDL<100
HDL>35
TAGs<150

35
Q

Tx recommendation for hyperlipidemia

A

6 mos no meds first and then HMG CoA reductase inhibitors if LDL>130 if over 10 and obese

36
Q

What is short stature?

A

Height 2 standard deviations below mean (<2.3 percentile)

37
Q

Most widely used system to measure skeletal age

A

Greulich-Pyle Atlas method

38
Q

Normal variants of growth leading to short stature

A

Familial short stature
Constitutional delay of growth (most common)
Idiopathic short stature
Small for age

39
Q

Pathologic Causes of growth failure

A 
Systemic disease
Endocrine (Cushings, hypothyroidism, GH deficiency, sexual precocity)
Genetic syndromes (turner, PWS, noonans, achondroplasia)
40
Q

What is familial short stature?

A

Kid is small b/c parents are short

Bone age is normal

41
Q

How to check mean parental height to consider familial short stature

A

Girls: 5 in taken off fathers height and avg with mom
Boys: 5 in added to mom and avg with dad

42
Q

What is constitutional delay of growth?

A

Later bloomers b/c late growth spurt
Bone is delayed and corresponds with height
Usually parents were delayed too

43
Q

How to diagnose GH deficiency

A

R/o hypothyroidism, turners and skeletal disorders

If none of them then do IGF-1, IGFBP-3, bone age (and maybe GH stimulation test)

44
Q

First line treatment for GH deficiency

A

Recombinant human growth hormone therapy (must be before growth plate closes)
Daily SC injections

45
Q

Side effects of rhGH

A

Psuedotumor cerebri
Hyperglycemia or insulin resistance
Gynecomastia
Increase T4 conversion without hypothyroidism

46
Q

What is Noonan syndrome?

A

Autosomal dominant
Short stature
CHD (pulmonic stenosis)
Variable genetic mutations

47
Q

Most common cause of pathologic obesity and short stature

A

PWS (chromosome 15)

48
Q

What is achondroplasia?

A

Autosomal dominant caused by mutations in FGFR3 gene (fibroblast growth factor)

49
Q

Features of achondroplasia

A

Disproportionate short stature with rhizomelic shortening-proximal bones shortened like humerus and femur
Macrocephaly
Normal cognition
Brachydactylyl and single transverse palmar crease

50
Q

Gigantism

A

GH excess prior to closure of epiphyses so excessive growth of long bones (rare compared to acromegaly)

51
Q

Diagnostics for GH excess

A

Increased serum IGF-1
GH suppression test (administer glucose and if GH fails to fall below 1 ng/mL then abnormal)
MRI to look at pituitary and hypo

52
Q

Tx for GH excess

A

Surgery, radiation,

Octreotide, bromocriptine

53
Q

Normal age of puberty

A

Boys 9-14 YO

Girls 8-14 YO

54
Q

Definition of precocious puberty

A

Onset of secondary sex characteristics before 8 in girls and before 9 in boys

55
Q

Central precocious puberty

A

Gonadotropin dependent to elevated GnRH and gonadotropins

Short stature

56
Q

Peripheral precocious puberty

A

Gonadotropin independent so elevated gonadal steroids with low gonadotropins

57
Q

Causes of central precocious puberty

A

Idiopathic mostly or CNS tumors or abnormalities

Girls

58
Q

Studies for central precocious puberty

A

LH and FSH high

Also do estradiol and testosterone

59
Q

Tx of central precocious puberty

A

GnRH analogue

60
Q

Causes of peripheral precocious puberty

A

Exposure to gonadal steroids outside of HPG axis
Congenital adrenal hyperplasia
McCune albright Syndrome (females)
*normal LH, FSH levels

61
Q

What is pubertal gynecomastic?

A

Benign

62
Q

Causes of prepubertal gynecomastia

A

Klinefelters
Aromatization due to obesity
Adrenal or testicular neoplasm

63
Q

Most common cause of contra sexual development

A

Congenital adrenal hyperplasia

64
Q

Most common reason for congenital adrenal hyperplasia

A

21 hydroxylase deficiency

X Pediatrics 2 (10 decks)

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